Single-step genome-wide association analyses of claw horn lesions in Holstein cattle using linear and threshold models.
Single-step genome-wide association analyses of claw horn lesions in Holstein cattle using linear and threshold models.
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DOI：
10.1186/s12711-023-00784-4
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发表时间：
2023-03-10
影响因子：
4.1
通讯作者：
Banos, Georgios
中科院分区：
文献类型：
--
作者：
Li, Bingjie;Barden, Matthew;Kapsona, Vanessa;Sanchez-Molano, Enrique;Anagnostopoulos, Alkiviadis;Griffiths, Bethany Eloise;Bedford, Cherril;Dai, Xiaoxia;Coffey, Mike;Psifidi, Androniki;Oikonomou, Georgios;Banos, Georgios
奶牛跛行主要由足部病变引起，包括蹄角病变（CHL）、蹄出血（SH）、蹄溃疡（SU）和白色线病（WL）。本研究基于CHL易感性和严重程度的详细动物表型，调查了三种CHL的遗传结构。遗传参数和育种值的估计，单步全基因组关联分析，和功能富集分析进行。所研究的性状受遗传控制，具有低至中等的遗传力。SH和SU易感性的遗传度估计值分别为0.29和0.35。SH和SU严重程度的遗传度分别为0.12和0.07。WL的遗传力相对较低，表明环境对WL的发生和发展的影响比其他两种CHL更大。SH和SU之间的遗传相关性很高（病变易感性为0.98，病变严重程度为0.59），而SH和SU与WL的遗传相关性也趋于正相关。候选数量性状位点（QTL）被确定为所有CHL，包括一些牛染色体（BTA）3和18与潜在的多效性效应与多足病变性状。BTA 3基因组窗口为0.65 Mb，分别解释SH易感性、SH严重性、WL易感性和WL严重性的遗传方差的0.41%、0.50%、0.38%和0.49%。BTA 18的另一个窗口分别解释了SH易感性、SU易感性和SU严重程度的0.66%、0.41%和0.70%的遗传方差。与CHL相关的候选基因组区域含有与免疫系统功能和炎症反应、脂质代谢、钙离子活性和神经元兴奋性相关的注释基因。所研究的CHL是具有多基因遗传模式的复杂性状。大多数性状表现出遗传变异，表明动物对CHL的抗性可以通过育种来提高。各性状间存在显著的正相关关系，这将有利于从整体上进行抗赤霉病的遗传改良。与SH、SU和WL的病变易感性和严重程度相关的候选基因组区域提供了对CHL潜在遗传背景的全球概况的见解，并为旨在增强奶牛足部健康的遗传改良计划提供了信息。在线版本包含补充材料，可通过10.1186/s12711-023-00784-4获得。
Lameness in dairy cattle is primarily caused by foot lesions including the claw horn lesions (CHL) of sole haemorrhage (SH), sole ulcers (SU), and white line disease (WL). This study investigated the genetic architecture of the three CHL based on detailed animal phenotypes of CHL susceptibility and severity. Estimation of genetic parameters and breeding values, single-step genome-wide association analyses, and functional enrichment analyses were performed. The studied traits were under genetic control with a low to moderate heritability. Heritability estimates of SH and SU susceptibility on the liability scale were 0.29 and 0.35, respectively. Heritability of SH and SU severity were 0.12 and 0.07, respectively. Heritability of WL was relatively lower, indicating stronger environmental influence on the presence and development of WL than the other two CHL. Genetic correlations between SH and SU were high (0.98 for lesion susceptibility and 0.59 for lesion severity), whereas genetic correlations of SH and SU with WL also tended to be positive. Candidate quantitative trait loci (QTL) were identified for all CHL, including some on Bos taurus chromosome (BTA) 3 and 18 with potential pleiotropic effects associated with multiple foot lesion traits. A genomic window of 0.65 Mb on BTA3 explained 0.41, 0.50, 0.38, and 0.49% of the genetic variance for SH susceptibility, SH severity, WL susceptibility, and WL severity, respectively. Another window on BTA18 explained 0.66, 0.41, and 0.70% of the genetic variance for SH susceptibility, SU susceptibility, and SU severity, respectively. The candidate genomic regions associated with CHL harbour annotated genes that are linked to immune system function and inflammation responses, lipid metabolism, calcium ion activities, and neuronal excitability. The studied CHL are complex traits with a polygenic mode of inheritance. Most traits exhibited genetic variation suggesting that animal resistance to CHL can be improved with breeding. The CHL traits were positively correlated, which will facilitate genetic improvement for resistance to CHL as a whole. Candidate genomic regions associated with lesion susceptibility and severity of SH, SU, and WL provide insights into a global profile of the genetic background underlying CHL and inform genetic improvement programmes aiming at enhancing foot health in dairy cattle. The online version contains supplementary material available at 10.1186/s12711-023-00784-4.
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影响因子：
3.5
作者：
Buch, L. H.;Sorensen, A. C.;Sorensen, M. K.
通讯作者：
Sorensen, M. K.
影响因子：
3.5
作者：
Croue, Iola;Michenet, Alexis;Ducrocq, Vincent
通讯作者：
Ducrocq, Vincent
影响因子：
3.5
作者：
Bicalho, R. C.;Cheong, S. H.;Guard, C. L.
通讯作者：
Guard, C. L.
影响因子：
3.5
作者：
Haggman, J.;Juga, J.
通讯作者：
Juga, J.
影响因子：
3.7
作者：
Lai E;Danner AL;Famula TR;Oberbauer AM
通讯作者：
Oberbauer AM